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NLRP3 炎性小体与宿主抵抗细菌感染。

NLRP3 inflammasome and host protection against bacterial infection.

机构信息

Department of Microbiology and Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon, Korea.

出版信息

J Korean Med Sci. 2013 Oct;28(10):1415-23. doi: 10.3346/jkms.2013.28.10.1415. Epub 2013 Sep 25.

Abstract

The inflammasome is a multi-protein complex that induces maturation of inflammatory cytokines interleukin (IL)-1β and IL-18 through activation of caspase-1. Several nucleotide binding oligomerization domain-like receptor family members, including NLRP3, recognize unique microbial and danger components and play a central role in inflammasome activation. The NLRP3 inflammasome is critical for maintenance of homeostasis against pathogenic infections. However, inflammasome activation acts as a double-edged sword for various bacterial infections. When the IL-1 family of cytokines is secreted excessively, they cause tissue damage and extensive inflammatory responses that are potentially hazardous for the host. Emerging evidence has shown that diverse bacterial pathogens or their components negatively regulate inflammasome activation to escape the immune response. In this review, we discuss the current knowledge of the roles and regulation of the NLRP3 inflammasome during bacterial infections. Activation and regulation of the NLRP3 inflammasome should be tightly controlled to prevent virulence and pathology during infections. Understanding the roles and regulatory mechanisms of the NLRP3 inflammasome is essential for developing potential treatment approaches against pathogenic infections.

摘要

炎症小体是一种多蛋白复合物,通过激活半胱天冬酶-1诱导白细胞介素(IL)-1β和IL-18 的成熟。几种核苷酸结合寡聚化结构域样受体家族成员,包括 NLRP3,识别独特的微生物和危险成分,并在炎症小体激活中发挥核心作用。NLRP3 炎症小体对于维持针对致病感染的体内平衡至关重要。然而,炎症小体激活对于各种细菌感染来说是一把双刃剑。当白细胞介素-1 细胞因子家族过度分泌时,它们会导致组织损伤和广泛的炎症反应,对宿主有潜在的危险。新出现的证据表明,多种细菌病原体或其成分通过负调控炎症小体激活来逃避免疫反应。在这篇综述中,我们讨论了 NLRP3 炎症小体在细菌感染过程中的作用和调节的最新知识。激活和调节 NLRP3 炎症小体应该受到严格控制,以防止感染过程中的毒力和病理学。了解 NLRP3 炎症小体的作用和调节机制对于开发针对致病感染的潜在治疗方法至关重要。

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